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HMOs and infections

corresponding

JANET FRICKER
Freelance medical writer, United Kingdom

Abstract

Human milk oligosaccharides (HMOs), found in breast milk, offer potential as new treatments for bacterial and viral infections. Mechanisms for the protective effects of HMOs include HMOs  (i)  selectively nourishing the growth of specific strains of bifidobacteria, thereby allowing the microbiota to outcompete pathogenic organisms, (ii) resemblance to cell surface glycan receptors as a result of which they (HMOs) bind to bacteria and viruses and inactivate them, and (iii) modulating the immune system by shifting T cell responses towards more balanced Th1/ Th2 cytokine production in the current review evidence is presented showing how the presence of the HMO lacto-N-difucohexaose I (LNDFHI) correlates with reduction in the growth of Group B streptococcus (GBS),  how the HMO lacto-N-neotetraose (LNnT)  is associated with reduced transmission of human immunodeficiency virus (HIV), and how HMOs could play a role in the fight against COVID-19.


Breastfed babies have decreased incidence of diarrhoea, respiratory, urinary tract, and ear infections, and are less likely to develop necrotizing enterocolitis (NEC) and sudden infant death syndrome, compared to formula fed babies (1). Paradoxically, human breast milk contains around 700 different species of bacteria (2), and   transmits a range of viruses including cytomegalovirus, rubella, human T-cell leukaemia virus (HTLV-1) and human immunodeficiency virus (HIV) (3). This paradox can be ascribed to the presence of human milk oligosaccharides (HMOs), complex carbohydrates found in human breast milk, which provide protection against certain bacteria and viruses.  

In the light of the antimicrobial properties of HMOs, efforts are currently  underway to study their action against SARS-CoV-2 (the causative organism of Covid-19).

 

Epidemiological evidence supports the concept of breast feeding providing protection against a wide range of infections. For example, the classic Dundee  < ... ...




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